Hidradenitis Suppurativa (HS) is a painful, chronic skin condition affecting areas where skin rubs together, such as the armpits, groin, and under the breasts. The condition begins when hair follicles become blocked, leading to the formation of deep, inflamed nodules, abscesses, and tunnels beneath the skin. These recurring lesions cause significant discomfort and scarring. This article examines the relationship between HS and systemic markers, focusing specifically on White Blood Cell (WBC) counts.
Hidradenitis Suppurativa and the Immune System
White Blood Cells (WBCs), also known as leukocytes, are an integral part of the body’s defense system. Originating in the bone marrow, they circulate throughout the blood and tissues. They are the primary responders to threats, mobilizing to injured areas to initiate defense and repair.
Hidradenitis Suppurativa (HS) is a disorder driven by a dysfunctional immune response focused on the hair follicles. The inflammation associated with HS is not simply a local skin issue; it involves a complex, dysregulated activation of both the innate and adaptive immune systems. This systemic involvement means the body is in a constant state of immune alertness, which has widespread effects beyond the skin lesions.
The pathology of HS involves the rupture of the hair follicle, which spills keratin and other follicular contents into the dermis, triggering a powerful inflammatory reaction. This event draws large numbers of various white blood cells, including neutrophils, lymphocytes, and monocytes, into the skin tissue. This continuous cycle of follicular blockage, rupture, and intense inflammation contributes to the progressive nature of the disease, leading to the formation of painful abscesses and the characteristic sinus tracts.
The Direct Link to Elevated White Blood Cells
Yes, HS can cause a sustained elevation in the White Blood Cell count, known as leukocytosis, due to the chronic, high-level systemic inflammation it causes. Since the disease is rooted in ongoing immune dysregulation, the body’s production of WBCs is constantly signaled to increase. Studies have shown that patients with HS frequently have higher odds of leukocytosis compared to healthy individuals, with the elevation being more pronounced in those with greater disease severity.
This chronic elevation is driven by an inflammatory cascade involving specific signaling proteins called cytokines. Pro-inflammatory cytokines, such as Tumor Necrosis Factor-alpha (TNF-α), Interleukin-1β (IL-1β), and Interleukin-17 (IL-17), are found at elevated levels in the lesions and often in the blood of HS patients. These chemical messengers signal the bone marrow to continuously ramp up the production and release of leukocytes into the bloodstream.
The leukocytosis seen in HS is typically dominated by an increase in specific white blood cell types, particularly neutrophils and monocytes. Neutrophils are the immune system’s first responders, and their sustained elevation reflects the body’s continuous effort to contain the inflammation and tissue damage within the skin lesions. Monocytes, which differentiate into macrophages at the site of inflammation, are also elevated, indicating the chronic nature of the tissue cleanup and remodeling process.
Distinguishing Inflammation from Infection
A high WBC count in a patient with HS requires careful interpretation because it can signify two different biological processes: the underlying chronic inflammation or a new, acute bacterial infection. The total WBC count alone is not enough to differentiate between these two causes, as both conditions can trigger a significant increase in circulating leukocytes. Acute infections, which frequently occur as secondary complications in HS lesions, cause a rapid and often higher spike in the WBC count than the chronic inflammation typically associated with the condition.
To determine the cause of the elevation, physicians rely on the complete blood count with differential, which breaks down the total WBC count into its specific cell types. Leukocytosis driven by the chronic inflammation of HS is often characterized by an increase in both neutrophils and monocytes, sometimes with intermediate elevations of C-reactive protein (CRP), a general marker of inflammation. However, an acute bacterial infection, such as a secondary infection of an open HS lesion, will typically cause a much sharper rise in the total WBC count, specifically due to a dramatic increase in the neutrophil count.
Furthermore, the clinical context is essential for interpretation; a sudden, pronounced increase in the WBC count, especially with a corresponding high fever or chills, points strongly toward an acute infection that needs immediate treatment. Other inflammatory markers, such as a significantly elevated C-reactive protein (CRP) level or Erythrocyte Sedimentation Rate (ESR), are also monitored to gauge the overall inflammatory activity. These combined laboratory and clinical findings allow the healthcare team to guide treatment, helping them decide whether the patient needs an adjustment to their ongoing anti-inflammatory therapy or a course of antibiotics for a secondary infection.